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The Fiber Disease

Human Anatomy, Physiology, and Medicine. Anything human!

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Postby codon blue » Mon Dec 11, 2006 12:46 pm

Hey everybody, here is some disturbing facts that have been bothering me for several years now. Maybe someone can give me their thoughts on its relevancy to our problem. Sorry for the length, but it is a complicated subject, so you may want to look further on your own.

It has to do with the codon triplets, mainly the "stop codons" in particular. Here is some information copied from the Wikipedia website. The pertinent info is in red. My comments are in blue.

The genome of an organism, is inscribed in DNA, or in some viruses RNA. The portion of the genome that codes for a protein or an RNA is referred to as a gene. Those genes that code for proteins are composed of tri-nucleotide units called codons, each coding for a single amino acid. Each nucleotide sub-unit consists of a phosphate, deoxyribose sugar and one of the 4 nitrogenous nucleotide bases. The purine bases adenine (A) and guanine (G) are larger and consist of two aromatic rings. The pyrimidine bases cytosine (C) and thymine (T) are smaller and consist of only one aromatic ring. In the double-helix configuration, two strands of DNA are joined to each other by hydrogen bonds in an arrangement known as base pairing. These bonds almost always form between an adenine base on one strand and a thymine on the other strand and between a cytosine base on one strand and a guanine base on the other. This means that the number of A and T residues will be the same in a given double helix as will the number of G and C residues. In RNA, thymine (T) is replaced by uracil (U), and the deoxyribose is substituted by ribose.

Each protein-coding gene is transcribed into a template molecule of the related polymer RNA, known as messenger RNA or mRNA. This in turn is translated on the ribosome into an amino acid chain or polypeptide. The process of translation requires transfer RNAs specific for individual amino acids with the amino acids covalently attached to them, guanosine triphosphate as an energy source, and a number of translation factors. tRNAs have anticodons complementary to the codons in mRNA and can be "charged" covalently with amino acids at their 3' terminal CCA ends. Individual tRNAs are charged with specific amino acids by enzymes known as aminoacyl tRNA synthetases which have high specificity for both their cognate amino acids and tRNAs. The high specificity of these enzymes is a major reasons why the fidelity of protein translation is maintained.

There are 4³ = 64 different codon combinations possible with a triplet codon of three nucleotides. In reality, all 64 codons of the standard genetic code are assigned for either amino acids or stop signals during translation. If, for example, an RNA sequence, UUUAAACCC is considered and the reading-frame starts with the first U (by convention,5' to 3'), there are three codons, namely, UUU, AAA and CCC, each of which specifies one amino acid. This RNA sequence will be translated into an amino acid sequence, three amino acids long.

Note that a codon is defined by the inital nucleotide from which translation starts. For example, the string GGGAAACCC, if read from the first position, contains the codons GGG, AAA and CCC;and if read from the second position, it contains the codons GGA and AAC; if read starting from the third position, GAA and ACC. Partial codons have been ignored in this example. Every sequence can thus be read in three reading frames, each of which will produce a different amino acid sequence (in the given example, Gly-Lys-Pro, Gly-Asp, or Glu-Thr, respectively). With double-stranded DNA there are six possible reading frames, three in the forward orientation on one strand and three reverse, or on the opposite strand.

The actual frame a protein sequence is translated in is defined by a start codon, usually the first AUG codon in the mRNA sequence. Mutations that disrupt the reading frame by insertions or deletions of one or two nucleotide bases are known as frameshift mutations. These mutations may impair the function of the resulting protein, if it is formed, and are thus rare in in vivo protein-coding sequences. Often such misformed proteins are targeted for proteolytic degradation. One reason for the rareness of frame-shifted mutations being inherited is that if the protein being translated is essential for growth under the selective pressures the organism faces, absence of a functional protein may cause lethality before the organism is viable.

Translation starts with a chain initiation codon (start codon). Unlike stop codons, the codon alone is not sufficient to begin the process. Nearby sequences and initiation factors are also required to start translation. The most common start codon is AUG, which also codes for methionine, but other start codons are also used.

The three stop codons have been given names: UAG is amber, UGA is opal (sometimes also called umber), and UAA is ochre. "Amber" was named after its discoverer Harris Bernstein, whose last name means "amber" in German. The other two stop codons were named 'ochre" and "opal" in order to keep the "color names" theme. Stop codons are also called termination codons and they signal release of the nascent polypeptide from the ribosome due to binding of release factors in the absence of cognate tRNAs with anticodons complementary to these stop signals.[2]

Numerous variations of the standard genetic code are found in mitochondria, which are energy-producing organelles that are found inside eukaryotic cells. Mycoplasma translate the codon UGA as tryptophan. Ciliate protozoa also have some variation in the genetic code: UAG and often UAA code for glutamine (a variant also found in some green algae), <why is that not surprising?>or UGA codes for cysteine. Another variant is found in some species of the yeast, Candida, where CUG codes for serine. In addition in some rare cases certain proteins may also use alternate initiation (start) codons.

In certain proteins, non-standard amino acids are substituted for standard stop codons, depending upon associated signal sequences in the messenger RNA: UGA can code for selenocysteine and UAG can code for pyrrolysine as discussed in the relevant articles. A detailed description of variations in the genetic code can be found at the NCBI web site. However, there may be other non-standard interpretations that are not yet known. Sequencing of genomes may reveal unique genetic codes that allow the incorporation of other novel amino acids into proteins.

True amber has sometimes been called kahroba, a word of Persian derivation signifying "that which attracts straw", in allusion to the power which amber possesses of acquiring an electric charge by friction. This property, first recorded by Thales of Miletus, suggested the word "electricity", from the Greek, elektron, a name applied, however, not only to amber but also to an alloy of gold and silver. By Latin writers amber is variously called electrum, sucinum (succinum), and glaesum or glesum. The Old Hebrew חשמל hashmal seems to have meant amber, although Modern Hebrew uses Arabic-inspired ענבר `inbar while חשמל hashmal means electricity.

Ochre or Ocher is a color, usually described as golden-yellow or light yellow brown. As a painting pigment it exists in at least four forms:

Yellow ochre, Fe2O3 • H2O, a hydrated Iron oxide
Red ochre, Fe2O3, chemically identical to yellow ochre, but reddened through heating
Purple ochre, identical to red ochre chemically but of a different hue caused by different light diffraction properties associated with a greater average particle size
Brown ochre (Goethite), also partly hydrated iron oxide (rust)
For further information, see the articles on the individual ochres. They are found throughout the world in many shades. Many sources consider the best brown ochre to come from Cyprus, and the best yellow and red ochre from Roussillon, France. All have been used since prehistoric times, and are some of oldest pigments used.

The mineraloid opal is amorphous SiO2·nH2O; hydrated silicon dioxide, <Another coincidence?" I think not!!>the water content sometimes being as high as 20% but is usually between three and ten percent. Opal ranges from colorless through white, milky blue, gray, red, yellow, green, brown and black. Common opal is truly amorphous, but precious opal does have a structural element. The word opal comes from the Sanskrit upala, the Greek opallios, and the Latin opalus, meaning "precious stone."

Opal is a mineraloid gel which is deposited at relatively low temperature and may occur in the fissures of almost any kind of rock, being most commonly found with limonite, sandstone, rhyolite, and basalt.

Opal is one of the mineraloids that can form or replace fossils. The resulting fossils, though not of any extra scientific interest, appeal to collectors.

I suggest that the implications here are staggering, please somebody tell me that I am wrong about this.
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Postby Maggie Mae » Mon Dec 11, 2006 1:40 pm

Thanks for the insight Deena. My reasons to file a law suit....whether provable or not....Time frame, documented cases, history records...we may be setting precidents. The money, yeah, I haven't left reality completely...I know the high wall, but I also know about Joshua.
I testified in front of a congressional hearing panel with regards to what was taking place in our area....spraying, poisoning, etc...that was some minor satisfaction. I also know I DID SOMETHING. We did not win, it cost us way too much that as you - did not have to spare....but, my kids are grown now, remembering their mother did not hide or roll over. They have strength, lots of it...and no doubt will need it down the pike. I feel that all the fibers, insects, and little bots I have collected are evidence as well as Sabrina's view....I can obtain them FRESH, on demand. I know about protocols, credible court evidence, yada...
they creeps stole almost every record, through certified mail, labs, etc...I have all the records, excuses, the "gees, dunno where they went..." we'll re-do them...6 months, 10 months, subpoenaes to the USDA, to get their findings, and yes, I am not afraid of losing anything....
I just have some gut feeling there is a Time Frame involved here, don't know how to logically explain, only that "someone" is telling me that it would be PRUDENT to take some steps...so I will pursue. Even if it is only a smoking gun...as I see it, "Ya got nothing, ya got nothing to lose" ~Dylan.
Besides, it is the ONLY thing I can do at this point...(besides give it to the Lord)
At one point til about 3 months ago, I could advance search on nuspa pages and copy from cache....they got those, too...wonder why it would be so important to remove......
And as I said previously, Bowen Labs have been involved with this since the beginning....OSU....I am sorry but that is truth....Dead friends don't lie. The creeps are stalling............now the question and I hate to really know the answer, is WHY.
Mm
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Postby Maggie Mae » Mon Dec 11, 2006 1:42 pm

BTW, has anyone else's e mails been re-directed? My friends, family weren't getting their e mails...got into a showdown with Yahoo...they finally e mailed me saying they were going to "Cornell" first to determine if they were spam or not.......LLLLLLLLLLLLLLOOOOOOOOOOOOOLLLLLLLLLLLL!! Do not be afraid of those that can kill the body, rather fear him who can kill both body and soul.

Mm
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Postby Maggie Mae » Mon Dec 11, 2006 1:44 pm

The lawyer put up his own firm's money...he told me that Monsanto depositioned him in Alaska, and Hawaii both in the same week....it was expensive as hell to pursue for him....but as I said, it's about being on file at the moment...(for Deena)
Mm
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Postby tamtam » Mon Dec 11, 2006 2:47 pm

Codon Blue wrote: "I suggest that the implications here are staggering, please somebody tell me that I am wrong about this"

You think about a petrified replica of an entity?
Last edited by tamtam on Mon Dec 11, 2006 3:03 pm, edited 1 time in total.
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Postby mfromcanada » Mon Dec 11, 2006 2:55 pm

codonblue, I wish I could understand your post but my spidy senses are up and I think you have something.
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Postby Maggie Mae » Mon Dec 11, 2006 3:14 pm

Hooop, here it is.................

http://www.google.com/search?q=Rhinospo ... &hl=en&lr=
Mm
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Postby Maggie Mae » Mon Dec 11, 2006 3:16 pm

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Postby Deena » Mon Dec 11, 2006 3:17 pm

Maggie Mae wrote:BTW, has anyone else's e mails been re-directed? My friends, family weren't getting their e mails...got into a showdown with Yahoo...they finally e mailed me saying they were going to "Cornell" first to determine if they were spam or not.......LLLLLLLLLLLLLLOOOOOOOOOOOOOLLLLLLLLLLLL!! Do not be afraid of those that can kill the body, rather fear him who can kill both body and soul.

Mm

COPY THIS , YES and I WROTE DOWN THE SEVERE CODE THAT TAGGED IT JUST BEFORE I 86'D ITS ASS

I 'D HAVE TO DIG THRU MY PILE HERE IN FRONT OF ME, TO FIND IT...
I WORK MUCH HARDER, THAN IT APPEARS> I JUST DON'T POST IT
THESE LAST FEW MESSAGES IS EXACTLY WHY!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!



GAME ON!!!!


HEY EVERYONE ...................DRAW YOUR WEAPONS!!!!!!!!
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Postby tamtam » Mon Dec 11, 2006 3:32 pm

Remember that it would concern a highly modified R. Seeberi and only if this highly modified R. Seeberi like micro organism consistently can be linked to microcystis
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Postby tamtam » Mon Dec 11, 2006 3:34 pm

The report of Levy et al that the organism from canine nasal rhinosporidiosis grew in cultures of human rectal epithelioid cells with the formation of polyps has had no independent confirmation.


Current Opinion in Infectious Diseases - Fulltext: Volume 18(2 ...Rhinosporidiosis may be regarded as an 'emerging infective disease' in ... Refutations of the Microcystis hypothesis were made in 2000 [6] and 2001 [7]. ...
http://www.co-infectiousdiseases.com/pt/re/coinfdis/ fulltext.00001432-200504000-00006.htm;jsessionid=FcVSn9W4QB2... - Similar pages
Rhinosporidiosis: what is the cause?.
Skin and soft tissue infections
Current Opinion in Infectious Diseases. 18(2):113-118, April 2005.
Arseculeratne, Sarath Nanda
Abstract: ?Purpose of review: Significant advances in knowledge on rhinosporidiosis and Rhinosporidium seeberi were made in 1999, 2000, 2003 and 2004. These advances are reviewed on account of the continuing sporadic occurrence of the disease universally, and because of the availability of new approaches that could resolve persisting enigmas of both the disease and its causative pathogen.
Recent findings: R. seeberi, the pathogen that causes rhinosporidiosis, has been definitively classified using molecular biological tools in a new clade - the Mesomycetozoea, along with 10 parasitic and saprobic microbes. The controversial spherical bodies of the endospores have been shown to comprise both lipid/protein nutritive bodies and other spherical bodies that are metabolizing units that reduce MTT (3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium bromide). This indicates the viability of these spherical bodies, provisionally identified as the electron dense bodies that have also been shown to contain nucleic acids. MTT reduction as an indicator of viability has been used to determine the sensitivity of rhinosporidial endospores to biocides, antimicrobial drugs, and to specific antibodies. Genetic heterogeneity has been identified in strains from humans and animals. Cell-mediated and humoral immune responses have been demonstrated in human patients and in mice. Several mechanisms of immune evasion by R. seeberi have been identified.
Summary: These findings are applicable in both clinical and laboratory practice, while the basic advances have implications in further work on experimental pathogenicity, the biology of R. seeberi, and on the epidemiology and pathogenesis of rhinosporidiosis.
(C) 2005 Lippincott Williams & Wilkins, Inc.
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Postby tamtam » Mon Dec 11, 2006 3:50 pm

Environmental Health: A Global Access Science Source | Full text ...
Many experimental models have utilised either in vitro studies of isolated cell lines or animal and human studies where LPS is exposed to the circulation by ...

http://64.233.183.104/search?q=cache:nG ... =clnk&cd=3
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